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Temporal changes in left ventricular function after massive sympathetic nervous system activation

S A Lang1, M B Maron, F J Bosso

  • 1Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown 44272.

Canadian Journal of Physiology and Pharmacology
|June 1, 1994
PubMed
Summary

Massive sympathetic nervous system (SNS) activation significantly reduces left ventricular (LV) contractility in dogs. This cardiac dysfunction occurs rapidly and persists, independent of initial blood pressure changes.

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Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Research

Background:

  • The sympathetic nervous system (SNS) plays a crucial role in regulating cardiac function.
  • Previous studies suggest SNS activation can impair left ventricular (LV) contractility.

Purpose of the Study:

  • To investigate the time course and characteristics of LV dysfunction following massive central SNS activation in dogs.
  • To differentiate the effects of SNS activation from mere hypertensive responses on LV contractility.

Main Methods:

  • Central SNS activation was induced via intracisternal veratrine injection in anesthetized dogs.
  • Hemodynamic parameters including LV end-diastolic pressure (LVEDP), cardiac output, heart rate, and aortic pressure (Pa) were monitored.
  • LV function curves were analyzed to assess contractility changes.

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  • Plasma catecholamine levels were measured.
  • Control groups included time-matched controls and dogs with aortic constriction to mimic hypertension.

    • Main Results:

    • Intracisternal veratrine rapidly increased aortic pressure and markedly decreased LV contractility, evidenced by shifts in LV function curves.
    • The observed LV dysfunction persisted for 3 hours, outlasting the initial hypertensive phase.
    • Plasma catecholamine concentrations significantly increased after SNS activation.
    • Aortic constriction alone resulted in only modest changes in LV function.

    Conclusions:

    • Massive SNS activation leads to a rapid and sustained decline in myocardial contractility.
    • The observed LV dysfunction is a direct consequence of SNS activation, not solely due to the associated hypertension.
    • Elevated catecholamines likely contribute to the observed myocardial depression.